TAP2 Antibody (N-Term)
Purified Rabbit Polyclonal Antibody (Pab)
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Application ![]()
| WB, FC, E |
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Primary Accession | Q03519 |
Reactivity | Human |
Host | Rabbit |
Clonality | polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 75664 Da |
Gene ID | 6891 |
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Other Names | Antigen peptide transporter 2, APT2, ATP-binding cassette sub-family B member 3, Peptide supply factor 2, Peptide transporter PSF2, PSF-2, Peptide transporter TAP2, Peptide transporter involved in antigen processing 2, Really interesting new gene 11 protein, TAP2, ABCB3, PSF2, RING11, Y1 |
Target/Specificity | This TAP2 antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 100-134 amino acids from the human region of human TAP2. |
Dilution | WB~~1:2000 FC~~1:25 E~~Use at an assay dependent concentration. |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | TAP2 Antibody (N-Term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | TAP2 {ECO:0000303|PubMed:10605026, ECO:0000312|HGNC:HGNC:44} |
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Function | ABC transporter associated with antigen processing. In complex with TAP1 mediates unidirectional translocation of peptide antigens from cytosol to endoplasmic reticulum (ER) for loading onto MHC class I (MHCI) molecules (PubMed:25377891, PubMed:25656091). Uses the chemical energy of ATP to export peptides against the concentration gradient (PubMed:25377891). During the transport cycle alternates between 'inward-facing' state with peptide binding site facing the cytosol to 'outward-facing' state with peptide binding site facing the ER lumen. Peptide antigen binding to ATP-loaded TAP1-TAP2 induces a switch to hydrolysis-competent 'outward-facing' conformation ready for peptide loading onto nascent MHCI molecules. Subsequently ATP hydrolysis resets the transporter to the 'inward facing' state for a new cycle (PubMed:11274390, PubMed:25377891, PubMed:25656091). Typically transports intracellular peptide antigens of 8 to 13 amino acids that arise from cytosolic proteolysis via IFNG-induced immunoproteasome. Binds peptides with free N- and C-termini, the first three and the C-terminal residues being critical. Preferentially selects peptides having a highly hydrophobic residue at position 3 and hydrophobic or charged residues at the C-terminal anchor. Proline at position 2 has the most destabilizing effect (PubMed:11274390, PubMed:7500034, PubMed:9256420). As a component of the peptide loading complex (PLC), acts as a molecular scaffold essential for peptide-MHCI assembly and antigen presentation (PubMed:1538751, PubMed:25377891, PubMed:26611325). |
Cellular Location | Endoplasmic reticulum membrane; Multi-pass membrane protein. Note=The transmembrane segments seem to form a pore in the membrane |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Involved in the transport of antigens from the cytoplasm to the endoplasmic reticulum for association with MHC class I molecules. Also acts as a molecular scaffold for the final stage of MHC class I folding, namely the binding of peptide. Nascent MHC class I molecules associate with TAP via tapasin. Inhibited by the covalent attachment of herpes simplex virus ICP47 protein, which blocks the peptide-binding site of TAP. Inhibited by human cytomegalovirus US6 glycoprotein, which binds to the lumenal side of the TAP complex and inhibits peptide translocation by specifically blocking ATP-binding to TAP1 and prevents the conformational rearrangement of TAP induced by peptide binding. Inhibited by human adenovirus E3-19K glycoprotein, which binds the TAP complex and acts as a tapasin inhibitor, preventing MHC class I/TAP association.
REFERENCES
Beck S.,et al.J. Mol. Biol. 228:433-441(1992).
Powis S.H.,et al.Proc. Natl. Acad. Sci. U.S.A. 89:1463-1467(1992).
Bahram S.,et al.Proc. Natl. Acad. Sci. U.S.A. 88:10094-10098(1991).
Powis S.H.,et al.Immunogenetics 37:373-380(1993).
Kumagai S.,et al.Arthritis Rheum. 40:1685-1692(1997).

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